The vestibular ocular reflex (VOR) is essential for normal vision because it reduces image motion on the retina during head movements. The visual capability of patients with VOR disorders is severely impaired by blurred and double vision. Although clinical tests for semicircular canal dysfunction are available, there are no standard clinical tests for otolith dysfunction and linear VOR deficiencies. Ocular compensation of translational head movements (the linear VOR) is more complex than compensation for rotatory head movements, and its neurophysiology is much less well understood. For the linear VOR, the direction and amplitude of compensatory eye movement depends on gaze direction, viewing distance, and the linear motion of the head. Unlike the angular VOR, there is no fixed relationship between the vestibular inflow and the motor output. The complex relationship of the linear VOR to gaze suggests that it is a behavior somewhere between reflexive and voluntary. The goal of this proposal is to elucidate the neurophysiological basis for the interaction of gaze information with otolith afferent signals that underlies the generation of motor commands to extraocular muscles for the linear VOR. To accomplish this goal, we will use single unit recording to quantitatively analyze central signals encoding linear motion and oculomotor variables in non-human primates. Two hypotheses will be rigorously evaluated. Hypothesis 1: Vestibular neurons that encode eye and head velocity in the same direction (Eye-Head Neurons) are essential components in linear VOR pathways. Eye-Head neurons will exhibit monocular eye movement related activity and encode gaze-modulated linear head movement signals. Hypothesis 2) Purkinje cells, located in the cerebellar flocculus/ventral paraflocculus will encode gaze-modulated linear head movement signals. In both structures, neurons will be organized according to eye movement direction and ocular selectivity. We will identify cells behaviorally, and determine their connectivity with the peripheral labyrinth and/or the cerebellum using electrical microstimulation. Our goal is to determine how networks of these cells transform vestibular afferent signals from the otoliths and central eye movement signals related to gaze into oculomotor commands.